I’ve often written that it’s hard to bring neuroscientific data to bear on issues in education (example here). Hard, but not impossible. Dorothy Bishop offered similar concerns on her blog Saturday. A study from Guinevere Eden’s lab provides a great example of how it can be done. It concerns the magnocellular theory of dyslexia (Stein, 2001). According to this theory, many varieties of reading disability have, at their core, a problem in the functioning of the magnocellular layer of the lateral geniculate nucleus of the thalamus. This layer of cells is known to be important in the processing of rapid motion, and people with developmental dyslexia are impaired on certain visual tasks entailing motion, such detecting coherent motion amongst a subset of randomly moving dots, or discriminating speeds of objects. The most widely accepted theory of reading disability points to a problem in phonological awareness—hearing individual speech sounds. The magnocellular theory emphasizes that phonological processing does not explain all of the data. There are visual problems in dyslexia as well. Proponents point to problems like letter transpositions and word substitutions while reading, and to visuo-motor coordination problems (Stein & Walsh, 1997; see Figure below) although the pervasiveness of these symptoms are not uncontested.

Parts of the posterior parietal cortex heavily influenced by magnocellular projections (A) and expected consequences of magnocellular impairment observed in children with dyslexia (B). From Stein & Walsh (1997)

Consistent with this hypothesis are post-mortem findings of cell volume differences in the magnocellular layer of dyslexics (Livingstone et al, 2001), deficits in motion detection process in individuals with dyslexia (Cornelissen, et al., 1997) and brain imaging studies showing reduced activity in cortical motion detection areas that are closely linked to the magnocellular system (e.g., Demb et al, 1997). It’s certainly an interesting hypothesis, but the data have been correlational. Maybe learning to read somehow steps up magnocellular function. That’s where Eden and her team come in. They compared kids with dyslexia to kids with typical reading development and found (as others have), reduced processing in motion detection cortical area V5. But then they compared kids with dyslexia to kids who were matched for reading achievement (and were therefore younger). Now there were no V5 differences between groups. These data are inconsistent with the idea that kids with dyslexia have an impaired magnocellular system. They are consistent with the idea that reading improves magnocellular function. (Why? A reasonable guess would be that reading requires rapid shifts of visual attention). In a second experiment, the researchers trained kids with dyslexia with a standard treatment protocol that focused on phonological awareness. V5 activity—which, again, is a cortical area concerned with motion processing--increased after the training! This result too, is consistent with the interpretation that reading prompts changes in magnocellular function. These are pretty compelling data indicating that reading disability is not caused by a congenital problem in magnocellular functioning. We see differences in motion detection between kids with and without dyslexia because reading improves the system’s functioning. The finding is interesting enough on its own, but I also want to point out that it’s a great example of how neuroscientific data can inform problems of interest to educators. About a year ago I wrote a series of blogs about techniques to solve this difficult problem. Eden’s group used a technique where brain activation is basically used as a dependent measure. Based on prior findings, researchers confidently interpreted V5 activity as a proxy for cognitive activity for motion processing. Indistinguishable V5 activity (compared to reading-matched controls) was interpreted as a normally operating system to detect motion. And therefore, not the cause of reading disability. I’m going out of my way to point out this success because I’ve so often said in the past that neuroscience applied to education has mostly been empty speculation, or the coopting of behavioral science with neuro-window-dressing. And I don’t want educators to start abbreviating “brain science” as BS. References: Cornelissen, P., Richardson, A., Mason, A., Fowler, S., and Stein, J. (1995). Contrast sensitivity and coherent motion detection measured at photopic luminance levels in dyslexics and controls. Vision Research, 35, 1483–1494. Demb, J.B., Boynton, G.M., and Heeger, D.J. (1997). Brain activity in visual cortex predicts individual differences in reading performance. PNAS, 94, 13363–13366. Livingstone, M.S., Rosen, G.D., Drislane, F.W., and Galaburda, A.M. (1991). Physiological and anatomical evidence for a magnocellular defect in develop-mental dyslexia. PNAS, 88, 7943–7947 Stein, J. (2001). The magnocellular theory of developmental dyslexia. Dyslexia, 7, 12-36. Stein, J. & Walsh, V. (1997). To see but not to read: The magnocellular theory of dyslexia. Trends in Neurosciences, 20, 147-152.

Doug1943

1/27/2014 19:51:23

An extremely useful example of how to do it right.

In trying to combat the overwhelming tide of neurobabble, which floats on the lamentable general ignorance of many educators but is driven by the good old desire to make a dollar on the part of a few people, we need counter-examples of what real science actually is. And here is one.

But in my view their main quality is not so much to show applications of neuroscience to education, but rather applications of neuroscience to psychology. They are using neuroimaging in a clever way to answer questions framed at the cognitive level, which is quite remarkable. And yes, these questions are educationally relevant, although I don't think that they qualify as "educational neuroscience" in the canonical sense.

Thanks Daniel for this very clear post. But while I agree it is a nice example of how neuroimaging can help understand the nature of reading problems, there are still two niggling questions.
First, what are teachers to do with this information? You may think I am being unrealistic in expecting direct educational applications to flow from work in this field, but this expectation has been created by the enthusiasm for this approach. For instance, the Wellcome Trust's new funding initiative in 'Neuroscience and Education' states "Projects will only be funded if there is an explicit causal hypothesis relating a finding in neuroscience to a novel intervention" and "we are only interested in testing initiatives that are practical and affordable for schools."
see http://educationendowmentfoundation.org.uk/apply-for-funding/neuroscience-round
In this regard, I think the best we can say for this paper is that it cautions educators against using interventions that aim to improve reading by training magnocellular function. I don't know of any of these, but no doubt someone somewhere is marketing such a training program. It doesn't tell teachers what they should do to help children with reading problems - except insofar as it confirmed there are benefits from the behavioural reading intervention used in experiment 3.
Second, we have to ask, did this study need brain imaging to show what it showed? The initial findings on magnocellular function were obtained with behavioural tests. Wouldn't these have been adequate for showing the same pattern of results as were obtained in the scanner? I don't think the answer is an obvious yes, because I know all too well that psychophysical tests are difficult to do with young children, who may do poorly because they are inattentive or unmotivated. So activation of area MT/V5 could be a better index of magno function. But there are also unwanted factors that can affect results in a scanner, most notably movement artefact: I could not see any mention of how this was handled in this study, yet it is a source of increasing concern for studies with children who are young or who have developmental problems.
I really don't want to seem like a Cassandra who rubbishes every attempt at doing neuroscientific studies of development or developmental disorders. Like Franck, I found much to like about this study. But my concern is that we are prioritising neuroscience approaches to developmental problems, and this is happening in part because researchers are offering the promise of educational relevance. In contrast, clinical trials of behavioural interventions, which have more potential for helping children, are much harder to fund, and are deemed far less exciting.

Elisabeth Whyte

1/28/2014 02:39:09

I think one thing Neuroscience can potentially help us understand whether interventions are directly having an impact in improving "typical" patterns of neural activation, or if they are engaging "compensatory" mechanisms that could have negative long-term consequences for future learning that is dependent on a solid foundation. I'm not sure that the actual science in practice can really clearly do that. Also, even if neuroscience can answer those questions, there is still no direct path from neuroscience to have direct relevance to the classroom. So, yes, while the intervention research we're doing is going to end up with a neuroscience component just because that's what is needed to catch the eye of funders, it could potentially be done just as well without the neuroscience component. Imaging testing around interventions helps teach us about how the brain works when the brain is learning, but teaches us very little about things that have direct classroom practical implications.